Protein kinase C-δ regulates the stability of hypoxia-inducible factor-1α under hypoxia

被引:27
作者
Lee, Ji-Won
Park, Jeong Ae
Kim, Se-Hee
Seo, Ji Hae
Lim, Kyung-Joon
Jeong, Joo-Won
Jeong, Chul-Ho
Chun, Kwang-Hoon
Lee, Seung-Ki
Kwon, Young-Guen
Kim, Kyu-Won [1 ]
机构
[1] Seoul Natl Univ, Coll Pharm, Neurovasc Coordinat Res Ctr, Seoul 151742, South Korea
[2] Seoul Natl Univ, Coll Pharm, Res Inst Pharmaceut Sci, Seoul 151742, South Korea
[3] Anyang Univ, Coll Liberal Arts & Sci, Dept Marine Biotechnol, Inchon 417833, South Korea
[4] Kyung Hee Univ, Sch Med, Inst Biomed Sci, Dept Anat & Neurobiol, Seoul 130701, South Korea
[5] Yonsei Univ, Coll Sci, Dept Biochem, Seoul 120749, South Korea
关键词
D O I
10.1111/j.1349-7006.2007.00535.x
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Hypoxia is a state of deficiency of available oxygen in the blood and tissues, and it occurs during several pathophysiological processes, including tumorigenesis. Under hypoxia, hypoxia-inducible factor-1 (HIF-1) plays an essential role in cellular oxygen homeostasis. In the present article protein kinase C-delta (PKC-delta) is activated by hypoxia, increases the protein stability and transcriptional activity of HIF-1 alpha in human cervical adenocarcinoma cells. Moreover, the knockdown of PKC-delta inhibited vascular endothelial growth factor expression and angiogenic activity under hypoxia. These effects were completely reversed by PKC-delta overexpression following the knockdown of PKC-delta. Collectively, these findings demonstrate the role of PKC-delta as a new regulator of hypoxia-induced angiogenesis.
引用
收藏
页码:1476 / 1481
页数:6
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